Pathophysiology of congestion and oedema Flashcards Preview

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Flashcards in Pathophysiology of congestion and oedema Deck (24):

Critical relationship

Q = ChangeinP/R

Q = blood flow
P = pressure
R = resistance


What is Congestion?

Relative excess of blood in vessels of tissue or organ:
- passive process
- Not like acute inflammation: active hyperaemia
- Acute or chronic


Clinical pathology examples

Local acute congestion
- Deep vein thrombosis

Local chronic congestion
- Hepatic cirrhosis

Generalised acute congestion
- Congestive cardiac failure


What is Deep vein thrombosis of the leg, and features?

- Vein blocked causing localised acute congestion
- Blood backs up in veins, venules, capillaries
- Decreased outflow of blood
- Local, acute congestion
- Decreased pressure gradient
- No O2 therefore ischaemia and infarction


What is Hepatic cirrhosis?

- Results from serious liver damage e.g. HBV, alcohol
- Regenerating liver forms nodules of hepatocytes with intervening fibrosis
- Loss of normal architecture: altered hepatic blood flow
- Portal blood flow blocked
- Local chronic congestion: haemorrhage risk


What are consequences of portal-systemic shunts?

- Caput medusae
- Oesophageal varices


Features of congestive cardiac failure

Heart unable to clear blood, right & left ventricles
- ineffective pump e.g. ischaemia, valve disease

Fluid (overload) in veins (Treatment: diuretics)


Pathophysiology of congestive cardiac failure

Decreased cardiac output (CO)

Decreased renal glomerular filtration rate (GFR)
- Activation of renin-angiotensin-aldosterone system
- Increased Na and H2O retention

Increased amount of fluid in body


What are effects of congestive cardiac failure?

- Heart cannot clear blood from ventricles

- Back pressure, blood dammed in veins

- Lungs -pulmonary oedema

- Liver: central venous congestion:
Right heart failure
Increased JVP, hepatomegaly, peripheral oedema


Pericentral hepatocytes and Periportal hepatocytes in hepatic central venous congestion

Pericentral hepatocytes (red) - Stasis of poorly oxygenated blood

Periportal hepatocytes (pale) - Relatively better oxygenated due to proximity of hepatic arterioles


What happens in normal microcirculation?

- Constant movement of fluid through capillary beds; process of dynamic equilibrium
- Driven by hydrostatic pressure from heart
- Balanced by osmotic pressures and endothelial permeability
- Filtration from capillary beds to interstitium
- Capillaries-interstitium-capillaries and lymphatics


Which three components affect net flux and filtration?

- Hydrostatic pressure
- Oncotic pressure
- Permeability characteristics and area of endothelium


What is Starling's hypothesis?

Net filtration (Jv)= [(force favouring filtration/flow of fluid out of vessel) - endothelial permeability to proteins x (forces opposing filtration/keeping fluid in vessel)] x endothelial permeability to H2O x area of capillary bed


What is normal oedema?

Accumulation of abnormal amounts of fluid in the extravascular compartment
- Intercellular tissue compartment (extracellular fluid)
- Body cavities


What is peripheral oedema?

Increased interstitial fluid in tissues


What are oedema effusions?

Fluid collections in body cavities
- Pleural, pericardial, joint effusions
- Abdominal cavity: ascites


What is Oedema: exudate?

- Part of inflammatory process due to increased vascular permeability
- Tumour, inflammation, allergy
- Higher protein/albumin content (cells)
- H2O & electrolytes
- High specific gravity


Pathophysiology of pulmonary oedema in left ventricular failure

Hydrostatic pressure - transudate

- Increased left atrial pressure > passive retrograde flow to pulmonary veins, capillaries and arteries
- Increased pulmonary vascular pressure
- Increased pulmonary blood volume
- Increased Pc > Increased filtration and pulmonary oedema


Pathophysiology of pulmonary oedema in lungs

- Perivascular and interstitial transudate
- Progressive oedematous widening of alveolar septa
- Accumulation of oedema fluid in alveolar spaces


Pathophysiology of peripheral oedema

Right heart failure – cannot empty RV in systole
Blood retained in systemic veins > Increased pressure in capillaries > increased filtration > peripheral oedema
also, secondary portal venous congestion via liver


Pathophysiology of peripheral oedema: Congestive cardiac failure

- Right and left ventricles both fail
- Pulmonary oedema and peripheral oedema at the same time
- All about hydrostatic pressure (P)


Pathophysiology of lymphatic blockage

Lymphatic obstruction - hydrostatic pressure upset
- Lymphatic drainage is required for normal flow
- If lymphatic system is blocked > lymphoedema
e.g. breast cancer may require radiotherapy to axilla > fibrosis > decreased outflow > oedema of upper limb


Pathophysiology of low protein oedema

Oncotic pressure - transudate
- Oncotic pressurec requires normal protein levels
- Hypoalbuminaemia > decreased oncotic pressurec > increases filtration
e.g nephrotic syndrome
e.g. hepatic cirrhosis
e.g. malnutrition


Pathophysiology of permeability oedema

Endothelial permeability - exudate

- Damage to endothelial lining > Increases "pores" in membrane > osmotic reflection coefficient of endothelium decreases towards zero

- Proteins and larger molecules can leak out (not just H2O)
e.g. acute inflammation such as pneumonia
e.g. burns